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针对阿尔茨海默病和相关 tau 病的 tau 去磷酸化靶向嵌合体的生成。

Generation of tau dephosphorylation-targeting chimeras for the treatment of Alzheimer's disease and related tauopathies.

机构信息

Department of Pathophysiology, School of Basic Medicine, Key Laboratory of Education Ministry of China/Hubei Province for Neurological Disorders, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China.

Department of Pathophysiology, School of Basic Medicine, Key Laboratory of Education Ministry of China/Hubei Province for Neurological Disorders, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China; School of Artificial Intelligence and Automation, Huazhong University of Science and Technology, Wuhan 430030, China.

出版信息

Sci Bull (Beijing). 2024 Apr 30;69(8):1137-1152. doi: 10.1016/j.scib.2024.01.019. Epub 2024 Jan 19.

Abstract

Abnormal hyperphosphorylation and accumulation of tau protein play a pivotal role in neurodegeneration in Alzheimer's disease (AD) and many other tauopathies. Selective elimination of hyperphosphorylated tau is promising for the therapy of these diseases. We have conceptualized a strategy, named dephosphorylation-targeting chimeras (DEPTACs), for specifically hijacking phosphatases to tau to debilitate its hyperphosphorylation. Here, we conducted the step-by-step optimization of each constituent motif to generate DEPTACs with reasonable effectiveness in facilitating the dephosphorylation and subsequent clearance of pathological tau. Specifically, for one of the selected chimeras, D16, we demonstrated its significant efficiency in rescuing the neurodegeneration caused by neurotoxic K18-tau seeds in vitro. Moreover, intravenous administration of D16 also alleviated tau pathologies in the brain and improved memory deficits in AD mice. These results suggested DEPTACs as targeted modulators of tau phosphorylation, which hold therapeutic potential for AD and other tauopathies.

摘要

异常过度磷酸化和 Tau 蛋白的积累在阿尔茨海默病 (AD) 和许多其他 Tau 病的神经退行性变中起着关键作用。选择性消除过度磷酸化的 Tau 蛋白有望成为这些疾病的治疗方法。我们提出了一种名为去磷酸化靶向嵌合体 (DEPTACs) 的策略,用于特异性劫持磷酸酶到 Tau 蛋白上,以削弱其过度磷酸化。在这里,我们逐步优化了每个组成基序,以生成具有合理有效性的 DEPTACs,促进病理性 Tau 蛋白的去磷酸化和随后的清除。具体来说,对于所选嵌合体之一 D16,我们证明了它在体外挽救神经毒性 K18-Tau 种子引起的神经退行性变方面的显著效果。此外,静脉注射 D16 还减轻了 AD 小鼠大脑中的 Tau 病理学并改善了记忆缺陷。这些结果表明 DEPTACs 是 Tau 蛋白磷酸化的靶向调节剂,具有治疗 AD 和其他 Tau 病的潜力。

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